Glaucoma is an ocular disorder associated with an elevated intraocular pressure which is too high for normal ocular function and may result in irreversible loss of visual function. If untreated, glaucoma may eventually lead to blindness. Ocular hypertension, that is, the condition of elevated intraocular pressure without optic nerve head damage or characteristic glaucomatous visual field defects, is now believed by many opthalmologists to represent the earliest phase of glaucoma.
Many of the drugs formerly used to treat glaucoma proved not entirely satisfactory. Indeed, few advances have been made in the treatment of glaucoma since pilocarpine and physostigmine were introduced for such treatment. Orally-administered carbonic anhydrase inhibitors are effective in some cases, and more recently topical beta-adrenergic blocking agents have been found to be effective in reducing intraocular pressure.
Although trifluoromethanesulfonamide and certain of its salts have been disclosed broadly in, for example, U.S. Pat. No. 2,732,398, Journal of the Chemical Society, 2640 (1957) and third International Fluorine Symposium, Munich (1965), their physiological activity as antiglaucoma agents has not previously been known.
Certain substituted haloalkanesulfonamides have previously been shown to have physiological activity as anticonvulsants. It has been theorized that since this activity is thought to be attributable to carbonic anhydrase activity, some of those compounds would also show activity against glaucoma. See U.S. Pat. Nos. 3,609,187, 3,622,626, and 3,705,185. However, prior art compounds, while they have been found to be active as antiglaucoma agents when administered orally, have been found to be inactive when administered topically.